beneath the table to the abstract. Use the Word Count cmd under Utilites menu for counting Significance Little information is available on embryo-maternal signaling during early pregnancy in primates. An increased understanding of the endocrine events that characterize this period in the nonhuman primate model will enhance our ability to monitor spontaneous and toxicant-induced pregnancy loss in humans. Objectives To study the endocrinology of early pregnancy loss induced by TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) in the cynomolgus monkey. The macaque exhibits similar endocrine and morphological characteristics during early pregnancy as described in humans and is sensitive to TCDD toxicity. Results Single doses of TCDD (1, 2, and 4 mg/kg) administered during early pregnancy resulted in fetal loss in the majority of animals (10/12). The primary endocrine alterations associated with fetal loss were decreases in serum estradiol and bioactive chorionic gonadotropin (CG) concentrations. Less pronounced decreases in serum progesterone, and relaxin were observed; there was no effect on immunoreactive CG. These results indicate that TCDD targets specific components of the CG synthetic machinery within the trophoblast to alter the functional capacity of the hormone. Moreover, these endocrine alterations occurred prior to overt signs of reproductive toxicity (i.e., early fetal loss). The relatively long interval from TCDD exposure to fetal loss (10-20 days) suggests that TCDD may have a direct toxic effect on the embryo. Future Directions Use of bioactive:immunoreactive CG ratio to monitor pregnancy outcome in human populations. KEY WORDS abortion, pregnancy, chorionic gonadotropin, estrogen, progesterone FUNDING NIH Grants ES06198 and RR00169